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Biomedical subjects

J C Floyd

Publications and source records attributed to J C Floyd.

At least 37 records · Page 2Linked to original sources

Release of human pancreatic polypeptide and gastrin in response to intraduodenal stimuli: a case report.

A recent clinical case afforded an opportunity to study the effects of duodenal stimulation on plasma human pancreatic polypeptide and gastrin concentrations, independent of gastric stimulation. A distension stimulus was provided by rapid injection of 100 ml of water and saline via a T-tube into an isolated duodenal afferent limb. In a third experiment, the saline contained 200 pg/ml of heptadecapeptide human gastrin. Within 2 min after each injection, a rapid rise in circulating human pancreatic polypeptide levels appeared that fell promptly towards basal thereafter. Injections of 100 ml of Flexical, a supplemental tube feeding, resulted in a biphasic human pancreatic polypeptide response, the initial peak comparable to that seen following distension with water, saline, or saline containing gastrin, and a second peak of much greater magnitude and duration followed the initial peak. Plasma gastrin concentrations were not influenced following any of the stimuli. Duodenal distension alone may induce an early transient increase in plasma human pancreatic polypeptide concentrations, while intraduodenal nutrients per se may induce a later increment of greater magnitude and duration.

Aged↗

Effect of age on fasting plasma levels of pancreatic hormones in man.

The effect of age and adiposity on fasting plasma levels of pancreatic polypeptide (HPP), glucagon (IRG), insulin (IRI) and glucose was examined in 263 healthy subjects between the ages of 20-69 yr. Mean plasma levels of hPP rose continuously from the third through the seventh decades. Mean plasma levels of IRG rose within the third and fourth decades but failed to rise further thereafter. Mean plasma levels of IRI did not change with age. Mean plasma levels of glucose rose by approximately 2 mg/dl . decade. The correlations of age with hPP, IRG, glucose, and adiposity were 0.47, 0.35, 0.25 (all P less than 0.01) and 0.15 (P less than 0.05), respectively. When adjustments were made for adiposity, the correlations of age with hPP, IRG, and glucose remained. Adiposity correlated with IRI, IRG, and glucose but when age correction was made, only the correlation of adiposity with IRI persisted. We conclude that: 1) age has a significant effect on fasting plasma levels of hPP and IRG; 2) the patterns of the age-related changes in hPP and IRG are not the same, suggesting that there are differences in the mechanism(s) by which age influences plasma levels of these two pancreatic hormones; and 3) age should be considered in the interpretation of fasting plasma levels of hPP and IRG.

Adult↗

Insulin, proinsulin, glucagon and gastrin in pancreatic tumors and in plasma of patients with organic hyperinsulinism.

Insulin, proinsulin, glucagon and gastrin were determined in extracts of tumors of 27 patients with pancreatic islet cell neoplasia of pancreas, in one patient with nesidioblastosis, in extracts of uninvolved portions of the pancreas in 11 of the tumor patients and of 15 control pancreases. Mean insulin concentration in solitary adenomas and in adenomas of patients with adenomatosis was higher than in control pancreases; however, in all but 1 patient the insulin concentration in neoplastic islet tissue was lower than in islet tissue of control pancreas, assuming islet volume is 1% of pancreas. The percentage of proinsulin was elevated in 52% of tumors. Adenoma insulin content correlated with increments of plasma insulin after tolbutamide administration. Insulin and proinsulin concentrations in pancreas uninvolved by tumor were not suppressed. Fasting plasma glucagon was elevated in patients with islet cell adenomatosis and in patients with islet cell carcinoma some of whom had multiple endocrine adenomatosis. The mean concentration of glucagon in tumors was lower than in control pancreases. Elevated concentration of gastrin was found in some adenomas. The data indicate: 1) insulin-secreting islet cell tumors have decreased storage capacity for insulin, 2) elevated concentration of proinsulin in tumors may be due to decreased capacity to store insulin and in some to decreased conversion of proinsulin to insulin as well, 3) tolbutamide stimulates the exaggerated release of a relatively constant fraction of insulin stored in adenomas. 4) solitary adenomas may contain excess amounts of pancreatic hormones in addition to insulin, 5) elevated plasma glucagon in patients with organic hyperinsulinism may indicate malignancy, microadenomatosis or multiple endocrine adenoma syndrome, and 6) chronic hyperinsulinism and hypoglycemia due to adenoma do not suppress insulin and proinsulin content of uninvolved pancreas.

Adenoma↗

The various faces of diabetes in the young: changing concepts.

Diabetes included several disorders associated with hyperglycemia. A difference in inheritance between the families of juvenile-onset- and maturity-onset-type diabetics, provides evidence for genetic heterogeneity. Heterogeneity of insulin responses to glucose was foung among nonobese patients with maturity-onset-type diabetes. Prospective studies in young patients have shown that glucose intolerance may not progress for as long as 22 years and that subnormal insulin responses to glucose have not decreased further, up to 12 years. However, patients who progressed to diabetes requiring insulin had insulin responses that were subnormal or below the control mean. None whose insulin responses exceeded this mean have decompensated. Thus, insulin response to glucose has prognostic implications. A tentative classification of diabetes in the young is proposed. There was a significant correlation between muscle capillary basement membrane width and known duration of carbohydrate intolerance.

Adolescent↗